Hello guys, as an engineer, I'm trying to find the most convenient and easisest idea to overcome this problem. This is just an idea, I'm not insisting my ideas are %100 true and admissible. All criticisms are very welcome.I always believe occam's razor. (https://en.wikipedia.org/wiki/Occam%27s_razor) That's the main belief when I created this theory.So, you know all SSRI's work in the same way. Blocking the Reuptake receptors, thus increase seratonin levels in the synaptics clefts. If we find/develope a chemical substance which make directly the opposite then maybe we can cure it? Of course, we will be very depressed, but in the end maybe we can be cured forever? What do you think?

Also, some people developed PSSD by taking only 1 pill! that means something definitely is switched off. If we do the right maneuver there will be opportunity to switch this thing back on in just one day.

Last edited by hgwxx7 on Fri Jun 29, 2018 3:06 pm, edited 1 time in total.

Tianeptine is a SSRE, but it’s some effects are same as SSRI’s.I think if they are not genetic changes, we could fix this with antagonizing ARs if antagonizing them not desensitizes them too.SSRI x —-> AR blocking ——> increasing serotoninCould x be mianserin?

Mianserin/Mirtazapine have been tried, i believe with limited success (mianserin worked for one person if im correct). But i really wonder if there is 1 case of PSSD, as cures dont seem to work for everyone.

A single paroxetine dose (1 mg/kg, i.p.) increased [5-HT](ext) over baseline in the frontal cortex and raphe nuclei, respectively. A single administration of tianeptine (10 mg/kg, i.p.) did not change [5-HT(ext)] in the two brain regions studied. Repeated exposure to paroxetine (0.5 mg/kg) b.i.d. for 14 days induced a sixfold significant increase in basal [5-HT](ext) in the raphe nuclei. Administration of tianeptine (5 mg/kg) b.i.d. for 14 days did not affect 5-HT baseline concentrations.